Our research assesses quantitatively the roles of membrane transport and of intracellular metabolism as rate determinants of the uptake of hexoses into animal cells. The strategy used is to compare the influx of a series of substrates of increasing metabolic complexity: a transported hexose which is metabolically inert, a hexose that is transported and phosphorylated, but not further metabolized and fully metabolized hexoses like glucose and fructose. Flux analysis is to be carried out with a temporal resolution sufficient to follow the time-courses of attainment of steady-states and, thus, to reveal the extent of rate limitation imposed at each of the early steps of hexose utilization and the apparent kinetic characteristics of a given step effective in situ. The cell systems to be examined from this perspective are normal rat hepatocytes versus Novikoff rat hepatoma cells and chick embryo cells versus their sarcoma virus-transformed counterparts. The comparison of results gathered with these cognate pairs will show which, or to what extent, each of these determinants are altered by oncogenic transformation. The information should help define quantitatively the role of the cell membrane as contributor to increased glycolysis in tumor cells--the much discussed, but poorly understood "Warburg effect." It is, thus, information prerequisite to an efficient search for the mechanism(s) of that effect, or the design of antineoplastic drugs which might exploit that effect.